Conditioning of the Myocardium

Abstract

Conditioning is the approach of protecting the myocardium and other cells, tissues, and organs against noxious stimuli, especially ischemia, by applying these stimuli in smaller strength and for a shorter time. It is being applied in different situations such as angina, myocardial infarction and in invasive procedures including angioplasty, TAVR, and cardiac surgery. It can be applied pre-, during and post- the harmful stimulus, and either locally or in remote organs or limbs. Although the clinical results are not overwhelming; it is still being intensively investigated.

Bolli R, Manchikalapudi S, Tang XL, Takano H, Qiu Y, Guo Y, et al. The protective effect of late preconditioning against myocardial stunning in conscious rabbits is mediated by nitric oxide synthase. Evidence that nitric oxide acts both as a trigger and as a mediator of the late phase of ischemic preconditioning. Circ Res. 1997;81:1094–107.PubMedCrossRefPubMedCentralGoogle Scholar

69.

Guo Y, Bao W, Wu WJ, Shinmura K, Tang XL, Bolli R. Evidence for an essential role of cyclooxygenase-2 as a mediator of the late phase of ischemic preconditioning in mice. Basic Res Cardiol. 2000;95:479–84.PubMedPubMedCentralCrossRefGoogle Scholar

Sivarajah A, McDonald MC, Thiemermann C. The production of hydrogen sulfide limits myocardial ischemia and reperfusion injury and contributes to the cardioprotective effects of preconditioning with endotoxin, but not ischemia in the rat. Shock. 2006;26:154–61.PubMedCrossRefPubMedCentralGoogle Scholar

Ovize M, Baxter GF, Di Lisa F, Ferdinandy P, Garcia-Dorado D, Hausenloy DJ, et al. Postconditioning and protection from reperfusion injury: where do we stand? Position paper from the working Group of Cellular Biology of the heart of the European society of cardiology. Cardiovasc Res. 2010;87:406–23.PubMedCrossRefPubMedCentralGoogle Scholar

Skyschally A, van Caster P, Boengler K, Gres P, Musiolik J, Schilawa D, et al. Ischemic postconditioning in pigs: no causal role for RISK activation. Circ Res. 2009;104:15–18. However, according to the same group activation showed that the phosphorylation of the RISK pathway does not reduce infarct size (113).PubMedCrossRefPubMedCentralGoogle Scholar

Heberden W A letter to Dr. Heberden concerning the angina pectoris: and an account of the dissection of the one who had been troubled by that disorder. Read at the college, Nov.17, 1772. Medical Transactions published by the College of Physicians in London 1785;3:1–11.Google Scholar

Williams DO, Bass TA, Gewirtz H, Most AS. Adaptation to the stress of tachycardia in patients with coronary artery disease: insight into the mechanism of the warm-up phenomenon. Circulation. 1985;71:687–92.PubMedCrossRefPubMedCentralGoogle Scholar